Nanoparticle-encapsulated Baicalin Inhibits Epithelial-mesenchymal Transition of Lung Cancer Cells Through PI3K/AKT/mTOR Pathway

Background Chemotherapy is the most important treatment for advanced lung cancer and epithelial-mesenchymal transition (EMT) involves in the drug resistance. Objectives Most lung cancer patients will develop drug resistance when they receive treatment, which is related to epithelial-mesenchymal transition (EMT) as a key mechanism that promotes the ability of lung cancer to invade and metastasize. Nanotechnology (NPs), as the main means of targeted delivery of drugs encapsulating baicalin (SA-SS-BAI) extracted from the traditional Chinese medicine Scutellaria baicalensis , plays anti-inflammatory and anti-tumor roles. However, the mechanism of the effect of SA-SS-BAI on EMT has not been clarified. This experiment mainly explores the inhibitory effect of SA-SS-BAI on EMT. Materials and Methods SA-SS-BAI NPs were prepared and observed by particle size, zeta potential, and transmission electron microscope. Human lung cancer cells (A549) were intervened. The A549 cells were assigned to three groups: the control group (Control), the baicalin group (BAI), and the baicalin nanoparticle group (SA-SS-BAI). The changes of SA-SS-BAI NPs on the expression of EMT marker proteins in A549 cells, cell apoptosis, proliferation, invasion, and migration were explored. Results SA-SS-BAI can inhibit the EMT of lung cancer cells. This inhibitory effect is mainly through the inhibiting of the phosphorylation of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), and mammalian target of rapamycin (mTOR), reducing cell proliferation, invasion, and migration while increasing the apoptosis rate of cells, and downregulating EMT marker proteins. Conclusion SA-SS-BAI can reduce the ability of lung cancer cells, increase the apoptosis rate, and inhibit the ability of EMT by reducing the activity of the PI3K/AKT/mTOR pathway.